Advanced Treatments Aiming to Stop the Development of Newborn Jaundice
A condition known as jaundice is responsible for many health risks and problems involving newborn babies, particularly in lesser developed countries throughout Africa and South Asia, where treatments such as blood transfusions are not as readily available as in developed countries.
Newborn jaundice is caused by the impairment of an enzyme that normally breaks down the molecule bilirubin after its heightened development right after birth. Although jaundice is harmless for the most part, merely causing the infant’s skin to turn temporarily yellow, higher concentration of bilirubin have also led to toxicity in the brain, and may lead to further complications or even death.
A New Study on the Source of Bilirubin Toxicity
Researchers working at the University of California and San Diego School of Medicine have recently identified a protein responsible for inhibiting the enzyme that normally regulates the breakdown of bilirubin. Their study, published in February b the Proceedings of the National Academy of Sciences focuses on an entirely new approach to treating jaundice that could lead to the development of easy to use, orally administered medicine for treating the problem.
Robert Tukey, PhD, one of the study’s co-authors, claims it to be the first report offering a clear and detailed description of the development of jaundice in newborns at a molecular level. Its purpose is the alleviating or possible prevention of bilirubin toxicity.
This disorder develops primarily when newborns are exposed to massive levels of oxygen right after birth, that their bodies find it difficult to handle. The destruction of red blood cells and excess bilirubin released in the bloodstream represent a temporary unbalance restored by the enzyme UGT1A1 (UDP-glucuronosyltransferase 1A1). When the enzyme is not capable of adequately performing in its role, the resulting high bilirubin concentration can lead to seizures, brain damage and possibly even death.
Identifying the Correct Treatment
Researcher Shujuan Chen, PhD, Robert Tukey’s collaborator on the project, has added the human version of the UGT1A1 gene to mice, studying and revealing how hyperbilirubinemia and its related health issues can develop. The team of researchers have found that, not only is the gene turned off in the liver – as in the case of human patients – but also impaired in the gastrointestinal tract. This important detail helped the scientists discover the real culprit: a repressor protein named NCoR1, or nuclear corepressor protein 1.
The simple act of deleting the NCoR1 gene from the gastrointestinal tissue in the humanized mice has resulted in the activation of the UCT1A1 gene. The enzyme proceeded to break down the exceeding amounts of bilirubin present in the body, and prevent the onset of neonatal hyperbilirubinemia.
Despite the importance and effectiveness of any future treatment leading to the same results, it is crucial to note that some of the effects of bilirubin toxicity are irreversible. As a result, the therapy has to be used in the early stages of hyperbilirubinemia, in order to prevent the onset of any of the severe secondary effects the disorder may be responsible for.
The good news, however, is that there is a good possibility of developing easy to administer oral therapeutics to help reactivate the enzyme and reduce excess bilirubin in time. The greatest challenge will be to reach as many of the more than 1 million newborns in the world that suffer every year from severe hyperbilirubinemia.